Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
J Intern Med. 2013 Apr;273(4):410-21. doi: 10.1111/joim.12032. Epub 2013 Feb 14.
Newly detected impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM) are common in patients with acute coronary syndrome (ACS; i.e. unstable angina/myocardial infarction) and related to disturbed beta-cell function. The aim of this study is to test the hypothesis that treatment with a dipeptidyl peptidase-4 inhibitor initiated soon after a coronary event improves beta-cell function.
Acute coronary syndrome ACS patients with IGT or T2DM (n = 71), screened by oral glucose tolerance test (OGTT) 4-23 days (median 6 days) after hospital admission, were randomly assigned to sitagliptin 100 mg (n = 34) or placebo (n = 37) and treated for a duration of 12 weeks. All patients received lifestyle advice but no glucose-lowering agents other than the study drug. The study end-point was beta-cell function assessed using the insulinogenic index (IGI = ΔInsulin30 /ΔGlucose30 ), derived from an OGTT, and acute insulin response to glucose (AIRg) assessed by a frequently sampled intravenous glucose tolerance test.
The IGI and AIRg did not differ at baseline between the sitagliptin and placebo groups (69.9 vs. 66.4 pmol mmol(-1) and 1394 vs. 1106 pmol L(-1) min(-1) respectively). After 12 weeks, the IGI was 85.0 in the sitagliptin and 58.1 pmol/mmol in the placebo group (P = 0.013) and AIRg was 1909 and 1043 pmol L(-1) min(-1) (P < 0.0001) in the sitagliptin and placebo groups respectively. Fasting glucose at baseline was 6.1 mmol L(-1) in sitagliptin-treated patients and 6.0 mmol L(-1) in those who received placebo compared with 5.8 and 5.9 mmol L(-1) respectively, after 12 weeks of treatment. Post load glucose metabolism improved in significantly more sitagliptin-treated patients compared with the placebo group (P = 0.003). Sitagliptin was well tolerated.
Sitagliptin improved beta-cell function and glucose perturbations in patients with ACS and newly diagnosed glucose disturbances.
急性冠状动脉综合征（ACS；即不稳定型心绞痛/心肌梗死）患者新发现的糖耐量受损（IGT）或 2 型糖尿病（T2DM）较为常见，且与β细胞功能紊乱有关。本研究旨在验证这样一个假设，即在冠状动脉事件后不久开始使用二肽基肽酶-4 抑制剂（DPP-4i）治疗可改善β细胞功能。
通过口服葡萄糖耐量试验（OGTT）在入院后 4-23 天（中位时间为 6 天）筛选出 IGT 或 T2DM 的 ACS 患者（n=71），将其随机分为西格列汀 100mg 组（n=34）或安慰剂组（n=37），并接受为期 12 周的治疗。所有患者均接受生活方式建议，但除研究药物外，不使用任何降糖药物。研究终点为使用 OGTT 得出的胰岛素原指数（IGI=ΔInsulin30/ΔGlucose30）评估β细胞功能，以及通过频繁采样静脉葡萄糖耐量试验评估急性胰岛素反应（AIRg）。
西格列汀组和安慰剂组的基线 IGI 和 AIRg 无差异（分别为 69.9 比 66.4 pmol mmol(-1)和 1394 比 1106 pmol L(-1) min(-1)）。12 周后，西格列汀组的 IGI 为 85.0，安慰剂组为 58.1 pmol/mmol（P=0.013），西格列汀组和安慰剂组的 AIRg 分别为 1909 和 1043 pmol L(-1) min(-1)（P<0.0001）。西格列汀治疗患者的空腹血糖基线为 6.1mmol L(-1)，而安慰剂组为 6.0mmol L(-1)，治疗 12 周后分别为 5.8 和 5.9mmol L(-1)。与安慰剂组相比，更多的西格列汀治疗患者的负荷后血糖代谢得到显著改善（P=0.003）。西格列汀耐受性良好。
西格列汀改善了 ACS 合并新发血糖紊乱患者的β细胞功能和血糖紊乱。
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